In general, the formation of gastric MALT lymphoma is based on the dependent and independent mechanisms of H. pylori infection; in H. pylori-dependent manner (in most cases), phosphorylated CagA inhibits p53 accumulation, whereas, in H. pylori-independent state, genetic aberrations lead to nuclear translocation of ‏API2–MALT1 chimeric transcript and BCL10, and eventually gastric MALT lymphoma [30, 68]. Here, BCL10 is linked to MALT lymphoma.